Journal articles: 'Excitotoxicity'

1

Nicotera, Pierluigi, and Marcel Leist. "Excitotoxicity." Cell Death & Differentiation 4, no. 6 (August 1997): 517–18. http://dx.doi.org/10.1038/sj.cdd.4400274.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Haglid, K. G., S. Wang, Y. Qiner, and A. Hamberger. "Excitotoxicity." Molecular Neurobiology 9, no. 1-3 (August 1994): 259–63. http://dx.doi.org/10.1007/bf02816125.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Rothstein, J. D. "Excitotoxicity hypothesis." Neurology 47, Issue 4, Supplement 2 (October 1, 1996): 19S—26S. http://dx.doi.org/10.1212/wnl.47.4_suppl_2.19s.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Novelli, A., and R. A. Tasker. "Excitotoxicity - Introduction." Amino Acids 23, no. 1-3 (September 1, 2002): 9–10. http://dx.doi.org/10.1007/s007260200028.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Stahl, Stephen M. "Excitotoxicity and Neuroprotection." Journal of Clinical Psychiatry 58, no. 6 (June 15, 1997): 247–48. http://dx.doi.org/10.4088/jcp.v58n0601.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Fernández-Sánchez, Maria Teresa, and Antonello Novelli. "Neurotrophins and Excitotoxicity." Science 270, no. 5244 (December 22, 1995): 2019. http://dx.doi.org/10.1126/science.270.5244.2019-a.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Nicholls, D. G., S. L. Budd, M. W. Ward, and R. F. Castilho. "Excitotoxicity and mitochondria." Biochemical Society Symposia 66 (September 1, 1999): 55–67. http://dx.doi.org/10.1042/bss0660055.

Full text

Abstract:

Excitotoxicity is the process whereby a massive glutamate release in the central nervous system in response to ischaemia or related trauma leads to the delayed, predominantly necrotic death of neurons. Excitotoxicity is also implicated in a variety of slow neurodegenerative disorders. Mitochondria accumulate much of the post-ischaemic calcium entering the neurons via the chronically activated N-methyl-d-aspartate receptor. This calcium accumulation plays a key role in the subsequent death of the neuron. Cultured cerebellar granule cells demonstrate delayed calcium de-regulation (DCD) followed by necrosis upon exposure to glutamate. DCD is unaffected by the ATP synthase inhibitor oligomycin but is inhibited by the further addition of a respiratory chain inhibitor to depolarize the mitochondria and inhibit mitochondrial calcium accumulation without depleting ATP [Budd and Nicholls (1996) J. Neurochem. 67, 2282-2291]. Mitochondrial depolarization paradoxically decreases the cytoplasmic calcium elevation following glutamate addition, probably due to an enhanced calcium efflux from the cell. Cells undergo immediate calcium de-regulation in the presence of glutamate if the respiratory chain is inhibited; this is due to ATP depletion following ATP synthase reversal and can be reversed by oligomycin. In contrast, DCD is irreversible. Elevated cytoplasmic calcium is not excitotoxic as long as mitochondria are depolarized; alternative substrates do not rescue cells about to undergo DCD, suggesting that glycolytic failure is not involved. Mitochondria in situ remain sufficiently polarized during granule cell glutamate exposure to continue to generate ATP and show a classic mitochondrial state 3-state 4 hyperpolarization on inhibiting ATP synthesis; mitochondrial depolarization follows, and may be a consequence of rather than a cause of DCD. In addition, our studies show no evidence of the mitochondrial permeability transition prior to DCD. The mitochondrial generation of superoxide anions is enhanced during glutamate exposure and a working hypothesis is that DCD may be caused by oxidative damage to calcium extrusion pathways at the plasma membrane.

APA, Harvard, Vancouver, ISO, and other styles

8

Leigh, P. N., and B. S. Meldrum. "Excitotoxicity in ALS." Neurology 47, Issue 6, Supplement 4 (December 1, 1996): 221S—227S. http://dx.doi.org/10.1212/wnl.47.6_suppl_4.221s.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Krieglstein, J. "Excitotoxicity and neuroprotection." European Journal of Pharmaceutical Sciences 5, no. 4 (July 1997): 181–87. http://dx.doi.org/10.1016/s0928-0987(97)00276-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Mohd Sairazi, Nur Shafika, K. N. S. Sirajudeen, Mohd Asnizam Asari, Mustapha Muzaimi, Swamy Mummedy, and Siti Amrah Sulaiman. "Kainic Acid-Induced Excitotoxicity Experimental Model: Protective Merits of Natural Products and Plant Extracts." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/972623.

Full text

Abstract:

Excitotoxicity is well recognized as a major pathological process of neuronal death in neurodegenerative diseases involving the central nervous system (CNS). In the animal models of neurodegeneration, excitotoxicity is commonly induced experimentally by chemical convulsants, particularly kainic acid (KA). KA-induced excitotoxicity in rodent models has been shown to result in seizures, behavioral changes, oxidative stress, glial activation, inflammatory mediator production, endoplasmic reticulum stress, mitochondrial dysfunction, and selective neurodegeneration in the brain upon KA administration. Recently, there is an emerging trend to search for natural sources to combat against excitotoxicity-associated neurodegenerative diseases. Natural products and plant extracts had attracted a considerable amount of attention because of their reported beneficial effects on the CNS, particularly their neuroprotective effect against excitotoxicity. They provide significant reduction and/or protection against the development and progression of acute and chronic neurodegeneration. This indicates that natural products and plants extracts may be useful in protecting against excitotoxicity-associated neurodegeneration. Thus, targeting of multiple pathways simultaneously may be the strategy to maximize the neuroprotection effect. This review summarizes the mechanisms involved in KA-induced excitotoxicity and attempts to collate the various researches related to the protective effect of natural products and plant extracts in the KA model of neurodegeneration.

APA, Harvard, Vancouver, ISO, and other styles

11

Zheng, Xiang-Yu, Hong-Liang Zhang, Qi Luo, and Jie Zhu. "Kainic Acid-Induced Neurodegenerative Model: Potentials and Limitations." Journal of Biomedicine and Biotechnology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/457079.

Full text

Abstract:

Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD). However, the mechanism by which excitotoxicity is implicated in neurodegenerative disorders remains unclear. Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS. KA has been extensively used as a specific agonist for ionotrophic glutamate receptors (iGluRs), for example, KARs, to mimic glutamate excitotoxicity in neurodegenerative models as well as to distinguish other iGluRs such asα-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors and N-methyl-D-aspartate receptors. Given the current knowledge of excitotoxicity in neurodegeneration, interventions targeted at modulating excitotoxicity are promising in terms of dealing with neurodegenerative disorders. This paper summarizes the up-to-date knowledge of neurodegenerative studies based on KA-induced animal model, with emphasis on its potentials and limitations.

APA, Harvard, Vancouver, ISO, and other styles

12

Liao, Rick, Thomas R. Wood, and Elizabeth Nance. "Nanotherapeutic modulation of excitotoxicity and oxidative stress in acute brain injury." Nanobiomedicine 7 (January 1, 2020): 184954352097081. http://dx.doi.org/10.1177/1849543520970819.

Full text

Abstract:

Excitotoxicity is a primary pathological process that occurs during stroke, traumatic brain injury (TBI), and global brain ischemia such as perinatal asphyxia. Excitotoxicity is triggered by an overabundance of excitatory neurotransmitters within the synapse, causing a detrimental cascade of excessive sodium and calcium influx, generation of reactive oxygen species, mitochondrial damage, and ultimately cell death. There are multiple potential points of intervention to combat excitotoxicity and downstream oxidative stress, yet there are currently no therapeutics clinically approved for this specific purpose. For a therapeutic to be effective against excitotoxicity, the therapeutic must accumulate at the disease site at the appropriate concentration at the right time. Nanotechnology can provide benefits for therapeutic delivery, including overcoming physiological obstacles such as the blood–brain barrier, protect cargo from degradation, and provide controlled release of a drug. This review evaluates the use of nano-based therapeutics to combat excitotoxicity in stroke, TBI, and hypoxia–ischemia with an emphasis on mitigating oxidative stress, and consideration of the path forward toward clinical translation.

APA, Harvard, Vancouver, ISO, and other styles

13

Ertugrul, Muhammed, Ufuk Okkay, Yesim Yeni, Sidika Genc, Ozge Balpinar, Irmak Okkay, and Ahmet Hacimuftuoglu. "Nicorandil mitigates glutamate excitotoxicity in primary cultured neurons." Medicine Science | International Medical Journal 13, no. 1 (2024): 43. http://dx.doi.org/10.5455/medscience.2023.07.112.

Full text

Abstract:

Excitotoxicity, caused by the excessive release of glutamate, leads to the activation of the apoptotic process, making it a crucial factor in age-related neurodegenerative diseases. The aim of this study was to investigate the potential of nicorandil to prevent glutamate excitotoxicity and reduce oxidative stress in the brain by analyzing the effects of nicorandil on primary cortex neurons. The study used primary neuron cultures from newborn Sprague-Dawley rats to examine the impact of nicorandil on cell viability, Superoxide Dismutase, Catalase, Glutathione activity, Malondialdehyde levels, total antioxidant capacity, and total antioxidant status of neurons subjected to glutamate-induced excitotoxicity. Nicorandil at varying concentrations was introduced in the culture to assess its protective effects on the neurons. The results showed that nicorandil significantly improved cell viability and total antioxidant capacity levels and reduced total antioxidant status values in a concentration-dependent manner. These findings indicate that nicorandil effectively prevented glutamate excitotoxicity by reducing oxidative stress. The study suggests that nicorandil holds the potential for treating neurodegenerative diseases caused by glutamate excitotoxicity. This study is the first to report the potential of nicorandil to inhibit oxidative stress and prevent glutamate excitotoxicity in primary neurons, providing a basis for further exploration of the clinical application of nicorandil in neurodegenerative diseases.

APA, Harvard, Vancouver, ISO, and other styles

14

Yalçın, G. Dönmez, and M. Colak. "SIRT4 prevents excitotoxicity via modulating glutamate metabolism in glioma cells." Human & Experimental Toxicology 39, no. 7 (February 21, 2020): 938–47. http://dx.doi.org/10.1177/0960327120907142.

Full text

Abstract:

Excitotoxicity is the presence of excessive glutamate, which is normally taken up by glutamate transporters on astrocytes. Glutamate transporter 1 (GLT-1) is the major transporter on glia cells clearing more than 90% of the glutamate. Sirtuin 4 (SIRT4) is a mitochondrial sirtuin which is expressed in the brain. Previously, it was shown that loss of SIRT4 leads to a more severe reaction to kainic acid, an excitotoxic agent, and also decreased GLT-1 expression in the brain. In this study, we aimed to investigate whether overexpression of SIRT4 is protective against excitotoxicity in glia cells. We overexpressed SIRT4 in A172 glioma cell line and treated with kainic acid in order to induce excitotoxicity. We observed that SIRT4 overexpression increased the cell viability after kainic acid treatment. In addition, reduced glutamate was detected in glutamate assay with overexpression of SIRT4 after kainic acid treatment since SIRT4 decreased cell death by preventing excitotoxicity. Our results show that overexpression of SIRT4 increased the protein levels of GLT-1 and glutamate dehydrogenase (GDH) after kainic acid (KA) treatment so that excess glutamate can be absorbed. However, overexpression of SIRT4 decreased glutamine synthetase (GS) levels. These results demonstrate that, by inhibiting GS, SIRT4 prevents glutamine formation, which will be converted to glutamate in neurons. SIRT4 prevents excitotoxicity via upregulating glutamate metabolism. Finally, our results may show that SIRT4 might prevent excitotoxicity and related cell death via reducing GS expression and upregulating GLT-1 and GDH levels. Therefore, it is important to develop therapeutics against excitotoxicity through SIRT4-related pathways in the cell.

APA, Harvard, Vancouver, ISO, and other styles

15

Zhuang, Dongli, Rong Zhang, Haiyang Liu, and Yi Dai. "A Small Natural Molecule S3 Protects Retinal Ganglion Cells and Promotes Parkin-Mediated Mitophagy against Excitotoxicity." Molecules 27, no. 15 (August 4, 2022): 4957. http://dx.doi.org/10.3390/molecules27154957.

Full text

Abstract:

Glutamate excitotoxicity may contribute to retinal ganglion cell (RGC) degeneration in glaucoma and other optic neuropathies, leading to irreversible blindness. Growing evidence has linked impaired mitochondrial quality control with RGCs degeneration, while parkin, an E3 ubiquitin ligase, has proved to be protective and promotes mitophagy in RGCs against excitotoxicity. The purpose of this study was to explore whether a small molecule S3 could modulate parkin-mediated mitophagy and has therapeutic potential for RGCs. The results showed that as an inhibitor of deubiquitinase USP30, S3 protected cultured RGCs and improved mitochondrial health against NMDA-induced excitotoxicity. Administration of S3 promoted the parkin expression and its downstream mitophagy-related proteins in RGCs. An upregulated ubiquitination level of Mfn2 and protein level of OPA1 were also observed in S3-treated RGCs, while parkin knockdown resulted in a major loss of the protective effect of S3 on RGCs under excitotoxicity. These findings demonstrated that S3 promoted RGC survival mainly through enhancing parkin-mediated mitophagy against excitotoxicity. The neuroprotective value of S3 in glaucoma and other optic neuropathies deserves further investigation.

APA, Harvard, Vancouver, ISO, and other styles

16

Hanley, Daniel F. "Multiple mechanisms of excitotoxicity." Critical Care Medicine 27, no. 3 (March 1999): 451–52. http://dx.doi.org/10.1097/00003246-199903000-00003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Stern, Peter. "Interface targeting skirts excitotoxicity." Science 370, no. 6513 (October 8, 2020): 182.16–184. http://dx.doi.org/10.1126/science.370.6513.182-p.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Raymond, Lynn A. "Excitotoxicity in Huntington disease." Clinical Neuroscience Research 3, no. 3 (September 2003): 121–28. http://dx.doi.org/10.1016/s1566-2772(03)00054-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Mayer, Mark L., and Gary L. Westbrook. "Cellular mechanisms underlying excitotoxicity." Trends in Neurosciences 10, no. 2 (February 1987): 59–61. http://dx.doi.org/10.1016/0166-2236(87)90023-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Matute, Carlos, Elena Alberdi, Gaskon Ibarretxe, and Marı́a Victoria Sánchez-Gómez. "Excitotoxicity in glial cells." European Journal of Pharmacology 447, no. 2-3 (July 2002): 239–46. http://dx.doi.org/10.1016/s0014-2999(02)01847-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Ikonomidou, Chrysanthy, and Lechoslaw Turski. "Excitotoxicity and neurodegenerative diseases." Current Opinion in Neurology 8, no. 6 (December 1995): 487. http://dx.doi.org/10.1097/00019052-199512000-00017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Whetsell, William O. "Current Concepts of Excitotoxicity." Journal of Neuropathology and Experimental Neurology 55, no. 1 (January 1996): 1–13. http://dx.doi.org/10.1097/00005072-199601000-00001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

GREENE, J., and J. GREENAMYRE. "Bioenergetics and glutamate excitotoxicity." Progress in Neurobiology 48, no. 6 (April 1996): 613–34. http://dx.doi.org/10.1016/0301-0082(96)00006-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Szydlowska, Kinga, and Michael Tymianski. "Calcium, ischemia and excitotoxicity." Cell Calcium 47, no. 2 (February 2010): 122–29. http://dx.doi.org/10.1016/j.ceca.2010.01.003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Leist, Marcel, and Pierluigi Nicotera. "Apoptosis, Excitotoxicity, and Neuropathology." Experimental Cell Research 239, no. 2 (March 1998): 183–201. http://dx.doi.org/10.1006/excr.1997.4026.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Johnston, Michael V. "Excitotoxicity in neonatal hypoxia." Mental Retardation and Developmental Disabilities Research Reviews 7, no. 4 (2001): 229–34. http://dx.doi.org/10.1002/mrdd.1032.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Yoshioka, Akira, Brian Bacskai, and David Pleasure. "Pathophysiology of oligodendroglial excitotoxicity." Journal of Neuroscience Research 46, no. 4 (November 15, 1996): 427–37. http://dx.doi.org/10.1002/(sici)1097-4547(19961115)46:4<427::aid-jnr4>3.0.co;2-i.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Aarts, Michelle M., Mark Arundine, and Michael Tymianski. "Novel concepts in excitotoxic neurodegeneration after stroke." Expert Reviews in Molecular Medicine 5, no. 30 (December 16, 2003): 1–22. http://dx.doi.org/10.1017/s1462399403007087.

Full text

Abstract:

Brain injury following cerebral ischaemia (stroke) involves a complex combination of pathological processes, including excitotoxicity and inflammation leading to necrotic and apoptotic forms of cell death. At the cellular level, excitotoxicity is mediated by glutamate and its cognate receptors, resulting in increased intracellular calcium and free radical production, and eventual cell death. Recent evidence suggests that scaffolding molecules that associate with glutamate receptors at the postsynaptic density allow coupling of receptor activity to specific second messengers capable of mediating excitotoxicity. These findings have important implications in the search for effective neuroprotective therapies in treating stroke.

APA, Harvard, Vancouver, ISO, and other styles

29

Han, Jin-Yi, Sun-Young Ahn, Eun-Hye Oh, Sang-Yoon Nam, Jin Tae Hong, Ki-Wan Oh, and Mi Kyeong Lee. "Red Ginseng Extract Attenuates Kainate-Induced Excitotoxicity by Antioxidative Effects." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/479016.

Full text

Abstract:

This study investigated the neuroprotective activity of red ginseng extract (RGE,Panax ginseng, C. A. Meyer) against kainic acid- (KA-) induced excitotoxicityin vitroandin vivo. In hippocampal cells, RGE inhibited KA-induced excitotoxicity in a dose-dependent manner as measured by the MTT assay. To study the possible mechanisms of the RGE-mediated neuroprotective effect against KA-induced cytotoxicity, we examined the levels of intracellular reactive oxygen species (ROS) and [Ca2+]iin cultured hippocampal neurons and found that RGE treatment dose-dependently inhibited intracellular ROS and [Ca2+]ielevation. Oral administration of RGE (30 and 200 mg/kg) in mice decreased the malondialdehyde (MDA) level induced by KA injection (30 mg/kg, i.p.). In addition, similar results were obtained after pretreatment with the radical scavengers Trolox andN,N′-dimethylthiourea (DMTU). Finally, after confirming the protective effect of RGE on hippocampal brain-derived neurotropic factor (BDNF) protein levels, we found that RGE is active compounds mixture in KA-induced hippocampal mossy-fiber function improvement. Furthermore, RGE eliminated 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, and the IC50was approximately 10 mg/ml. The reductive activity of RGE, as measured by reaction with hydroxyl radical (•OH), was similar to trolox. The second-order rate constant of RGE for•OH was 3.5–4.5×109 M−1·S−1. Therefore, these results indicate that RGE possesses radical reduction activity and alleviates KA-induced excitotoxicity by quenching ROS in hippocampal neurons.

APA, Harvard, Vancouver, ISO, and other styles

30

Ivanova, Svetlana A., and Anton J. M. Loonen. "Levodopa-Induced Dyskinesia Is Related to Indirect Pathway Medium Spiny Neuron Excitotoxicity: A Hypothesis Based on an Unexpected Finding." Parkinson's Disease 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/6461907.

Full text

Abstract:

A serendipitous pharmacogenetic finding links the vulnerability to developing levodopa-induced dyskinesia to the age of onset of Huntington’s disease. Huntington’s disease is caused by a polyglutamate expansion of the protein huntingtin. Aberrant huntingtin is less capable of binding to a member of membrane-associated guanylate kinase family (MAGUKs): postsynaptic density- (PSD-) 95. This leaves more PSD-95 available to stabilize NR2B subunit carrying NMDA receptors in the synaptic membrane. This results in increased excitotoxicity for which particularly striatal medium spiny neurons from the indirect extrapyramidal pathway are sensitive. In Parkinson’s disease the sensitivity for excitotoxicity is related to increased oxidative stress due to genetically determined abnormal metabolism of dopamine or related products. This probably also increases the sensitivity of medium spiny neurons for exogenous levodopa. Particularly the combination of increased oxidative stress due to aberrant dopamine metabolism, increased vulnerability to NMDA induced excitotoxicity, and the particular sensitivity of indirect pathway medium spiny neurons for this excitotoxicity may explain the observed increased prevalence of levodopa-induced dyskinesia.

APA, Harvard, Vancouver, ISO, and other styles

31

Kim, Gyung W., Jean-Christophe Copin, Makoto Kawase, Sylvia F. Chen, Shuzo Sato, Glenn T. Gobbel, and Pak H. Chan. "Excitotoxicity is Required for Induction of Oxidative Stress and Apoptosis in Mouse Striatum by the Mitochondrial Toxin, 3-Nitropropionic Acid." Journal of Cerebral Blood Flow & Metabolism 20, no. 1 (January 2000): 119–29. http://dx.doi.org/10.1097/00004647-200001000-00016.

Full text

Abstract:

Excitotoxicity is implicated in the pathogenesis of several neurologic diseases, such as chronic neurodegenerative diseases and stroke. Recently, it was reported that excitotoxicity has a relationship to apoptotic neuronal death, and that the mitochondrial toxin, 3-nitropropionic acid (3-NP), could induce apoptosis in the striatum. Although striatal lesions produced by 3-NP could develop through an excitotoxic mechanism, the exact relationship between apoptosis induction and excitotoxicity after 3-NP treatment is still not clear. The authors investigated the role of excitotoxicity and oxidative stress on apoptosis induction within the striatum after intraperitoneal injection of 3-NP. The authors demonstrated that removal of the corticostriatal glutamate pathway reduced superoxide production and apoptosis induction in the denervated striatum of decorticated mice after 3-NP treatment. Also, the N-methyl-d-aspartate (NMDA) receptor antagonist, MK-801, prevented apoptosis in the striatum after 3-NP treatment for 5 days, whereas the non-NMDA receptor antagonist, 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline, was ineffective. The authors also evaluated the initial type of neuronal death by 3-NP treatment for different durations from 1 to 5 days. In early striatal damage, apoptotic neuronal death initially occurred after 3-NP treatment. Our data show that excitotoxicity related to oxidative stress initially induces apoptotic neuronal death in mouse striatum after treatment with 3-NP.

APA, Harvard, Vancouver, ISO, and other styles

32

Chao, Hsiao-Ming, Ing-Ling Chen, and Jorn-Hon Liu. "S-Allyl L-Cysteine Protects the Retina Against Kainate Excitotoxicity in the Rat." American Journal of Chinese Medicine 42, no. 03 (January 2014): 693–708. http://dx.doi.org/10.1142/s0192415x14500451.

Full text

Abstract:

Excitotoxicity has been proposed to play a pivotal role in retinal ischemia. Retinal ischemia-associated ocular disorders are vision threatening. The aim was to also examine whether and how S-allyl L-cysteine (SAC) can protect the retina against kainate excitotoxicity. In vivo retinal excitotoxicity was induced by an intravitreous injection of 100 μM kainate into a Wistar rat eye for 1 day. The management and mechanisms involved in the processes were evaluated by electrophysiology, immunohistochemistry, histopathology, and various biochemical approaches. In the present study, the cultured retinal cells were shown to possess kainate receptors. The defined retinal excitotoxic changes were characterized by a decrease in electroretinogram (ERG) b-wave amplitudes, a loss of the fluorogold retrograde labeled retinal ganglion cells (RGCs), an increase in the apoptotic cells in the RGC layer, and an increase in vimentin or glial fibrillary acidic protein (GFAP) immunoreactivity, a marker for Müller cells. An up-regulation in the mRNA levels of inducible nitric oxide synthase (iNOS) and matrix metalloproteinases-9 (MMPs-9) was also detected in the retina subjected to kainate excitoxicity. Importantly, the excitotoxicity-induced alterations were significantly blunted when 100 μM SAC and/or the kainate receptor antagonist CNQX was applied. Conclusively, SAC would seem to protect the retina against kainate excitotoxicity via an inhibition of the up-regulation of iNOS and MMP-9 as well as a modulation of glial activation and apoptosis.

APA, Harvard, Vancouver, ISO, and other styles

33

Lu, Cheng-Wei, Chia-Chan Wu, Kuan-Ming Chiu, Ming-Yi Lee, Tzu-Yu Lin, and Su-Jane Wang. "Inhibition of Synaptic Glutamate Exocytosis and Prevention of Glutamate Neurotoxicity by Eupatilin from Artemisia argyi in the Rat Cortex." International Journal of Molecular Sciences 23, no. 21 (November 2, 2022): 13406. http://dx.doi.org/10.3390/ijms232113406.

Full text

Abstract:

The inhibition of synaptic glutamate release to maintain glutamate homeostasis contributes to the alleviation of neuronal cell injury, and accumulating evidence suggests that natural products can repress glutamate levels and associated excitotoxicity. In this study, we investigated whether eupatilin, a constituent of Artemisia argyi, affected glutamate release in rat cortical nerve terminals (synaptosomes). Additionally, we evaluated the effect of eupatilin in an animal model of kainic acid (KA) excitotoxicity, particularly on the levels of glutamate and N-methyl-D-aspartate (NMDA) receptor subunits (GluN2A and GluN2B). We found that eupatilin decreased depolarization-evoked glutamate release from rat cortical synaptosomes and that this effect was accompanied by a reduction in cytosolic Ca2+ elevation, inhibition of P/Q-type Ca2+ channels, decreased synapsin I Ca2+-dependent phosphorylation and no detectable effect on the membrane potential. In a KA-induced glutamate excitotoxicity rat model, the administration of eupatilin before KA administration prevented neuronal cell degeneration, glutamate elevation, glutamate-generating enzyme glutaminase increase, excitatory amino acid transporter (EAAT) decrease, GluN2A protein decrease and GluN2B protein increase in the rat cortex. Taken together, the results suggest that eupatilin depresses glutamate exocytosis from cerebrocortical synaptosomes by decreasing P/Q-type Ca2+ channels and synapsin I phosphorylation and alleviates glutamate excitotoxicity caused by KA by preventing glutamatergic alterations in the rat cortex. Thus, this study suggests that eupatilin can be considered a potential therapeutic agent in the treatment of brain impairment associated with glutamate excitotoxicity.

APA, Harvard, Vancouver, ISO, and other styles

34

Mironova, Yu S., I. A. Zhukova, N. G. Zhukova, V. M. Alifirova, O. P. Izhboldina, and A. V. Latypova. "Parkinson's disease and glutamate excitotoxicity." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 118, no. 6 (2018): 50. http://dx.doi.org/10.17116/jnevro201811806250.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Ong, Wei-Yi, Kazuhiro Tanaka, Gavin S. Dawe, Lars M. Ittner, and Akhlaq A. Farooqui. "Slow Excitotoxicity in Alzheimer's Disease." Journal of Alzheimer's Disease 35, no. 4 (May 21, 2013): 643–68. http://dx.doi.org/10.3233/jad-121990.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Huang, Chin-Wei, Ming-Chi Lai, Juei-Tang Cheng, Jing-Jane Tsai, Chao-Ching Huang, and Sheng-Nan Wu. "Pregabalin Attenuates Excitotoxicity in Diabetes." PLoS ONE 8, no. 6 (June 13, 2013): e65154. http://dx.doi.org/10.1371/journal.pone.0065154.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Jones, Rachel. "Blocking the pathway to excitotoxicity." Nature Reviews Neuroscience 3, no. 12 (December 2002): 916. http://dx.doi.org/10.1038/nrn992.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Dubinsky, J. M. "EXCITOTOXICITY AS A STOCHASTIC PROCESS." Clinical and Experimental Pharmacology and Physiology 22, no. 4 (April 1995): 297–98. http://dx.doi.org/10.1111/j.1440-1681.1995.tb02001.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

McEntee, William J. "Wernicke's Encephalopathy: an Excitotoxicity Hypothesis." Metabolic Brain Disease 12, no. 3 (September 1997): 183–92. http://dx.doi.org/10.1023/b:mebr.0000007099.18010.72.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Nilsen, Jon, Alison Morales, and Roberta Diaz Brinton. "Medroxyprogesterone acetate exacerbates glutamate excitotoxicity." Gynecological Endocrinology 22, no. 7 (January 2006): 355–61. http://dx.doi.org/10.1080/09513590600863337.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Zhou, Xianju, Zhuoyou Chen, Wenwei Yun, Jianhua Ren, Chengwei Li, and Hongbing Wang. "Extrasynaptic NMDA Receptor in Excitotoxicity." Neuroscientist 21, no. 4 (August 28, 2014): 337–44. http://dx.doi.org/10.1177/1073858414548724.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Olney, J. "Excitotoxicity, apoptosis and neuropsychiatric disorders." Current Opinion in Pharmacology 3, no. 1 (February 2003): 101–9. http://dx.doi.org/10.1016/s1471489202000024.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

OLNEY, J. "Excitotoxicity, apoptosis and neuropsychiatric disorders." Current Opinion in Pharmacology 3, no. 1 (February 2003): 101–9. http://dx.doi.org/10.1016/s1471-4892(02)00002-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Nicholls, David G., and Samantha L. Budd. "Mitochondria and neuronal glutamate excitotoxicity." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1366, no. 1-2 (August 1998): 97–112. http://dx.doi.org/10.1016/s0005-2728(98)00123-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Ludolph, A. C., M. Riepe, and K. Ullrich. "Excitotoxicity, energy metabolism and neurodegeneration." Journal of Inherited Metabolic Disease 16, no. 4 (1993): 716–23. http://dx.doi.org/10.1007/bf00711903.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Johnston, Michael V. "Excitotoxicity in Perinatal Brain Injury." Brain Pathology 15, no. 3 (April 5, 2006): 234–40. http://dx.doi.org/10.1111/j.1750-3639.2005.tb00526.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

van Cutsem, P., M. Dewil, W. Robberecht, and L. van den Bosch. "Excitotoxicity and Amyotrophic Lateral Sclerosis." Neurodegenerative Diseases 2, no. 3-4 (2005): 147–59. http://dx.doi.org/10.1159/000089620.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Flint Beal, M. "Huntington's disease, energy, and excitotoxicity." Neurobiology of Aging 15, no. 2 (March 1994): 275–76. http://dx.doi.org/10.1016/0197-4580(94)90132-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

McEntee, William J. "Wernicke’s encephalopathy: an excitotoxicity hypothesis." Metabolic Brain Disease 12, no. 3 (September 1997): 183–92. http://dx.doi.org/10.1007/bf02674611.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Izumi, Yukitoshi, Keiko Shimamoto, Ann M. Benz, Seth B. Hammerman, John W. Olney, and Charles F. Zorumski. "Glutamate transporters and retinal excitotoxicity." Glia 39, no. 1 (May 23, 2002): 58–68. http://dx.doi.org/10.1002/glia.10082.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Excitotoxicity'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles